Ultraviolet Light in Human Health, Diseases and Environment by Shamim I. Ahmad

Author:Shamim I. Ahmad
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

14.5.3 Vitamin D and Food Allergy

Epidemiological data have linked FA with sunlight exposure by showing that FA is more prevalent in regions further away from the equator [84, 85]. A recent study from Korea compared VD serum levels and the incidence of food induced anaphylaxis (FIA) between 2 regions of high and low solar radiation; VD levels were lower and concurrently FIA incidence was higher in the region with the low er solar radiation [65]. This kind of studies can lead to assumptions but cannot prove that FA is correlated to VD status and not to any other sunlight-derived, seasonal and/or geographic factor. However, they have provided a stimulating framework for further research on the subject [104]. Indeed, the research hypothesis of a connection between VD and FA has been largely corroborated by cross-sectional and cohort studies assessing VD dietary intake during pregnancy, or measuring maternal, cord blood, neonatal or childhood VD status. Sharief et al. used a large nationally representative sample from United States of more than 3000 children and adolescent, and found that VD deficiency was associated with allergic sensitization to selected foods. This association was not observed in the adult group of the study [112]. Similarly, in a cross-sectional study from Korea that included 226 infants with atopic dermatitis or FA it was found that VD deficiency increased the risk of food allergen sensitization [7]. In another large prospective cohort study conducted in Australia, infants with 25(OH)D < 50 nmol/l at 12 months of age were more likely to suffer from challenge-proven FA – especially to egg and peanut – and were more likely to have multiple food allergies compared with those with adequate VD levels [3]. Interestingly, this association was evident only among infants of Australian-born parents, suggesting a gene–environmental interaction [94].

Nwaru BI et al. showed that maternal intake of VD during pregnancy was associated with decreased risk of food sensitization in the offspring at the age of 5 years [89]. Chiu CY et al. demonstrated an inverse association between cord blood 25(OH)D levels from a birth cohort of Taiwanese children and milk sensitization at the age of 2 years [33]. However, there are also studies that failed to find a valid association between cord blood 25(OH)D levels and FA [29, 61]. Though not proving an association does not necessarily rule out its existence, their results have introduced some scepticism. What is more, a German study reported that maternal and cord blood 25(OH)D was positively associated with children’s risk for FA within the first 2 years of life. As a general comment, one could say that the presence of conflicting results reflects the gaps in our knowledge on the exact role of VD in the development of FA.

A proposed model of the induction of FA focuses on the actions of VD on the gastrointestinal tract which is the mucosal site with the richest antigenic exposure in the body. According to this model, VD deficiency not only compromises immune tolerance, but also increases susceptibility to infections and affects gut microbiota composition.

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